477-30-5

Faintly Yellow Crystalline Powder

An antimitotic agent that disrupts microtubles by binding to tubulin and preventing its polymerization. Stimulates the intrinsic GTPase activity of tubulin. Induces apoptosis in several normal and tumor cell lines and activates the JNK/SAPK signaling pathway.

Inhibitor of spindle fiber formation

ChEBI: A secondary amino compound that is (S)-colchicine in which the N-acetyl group is replaced by an N-methyl group. Isolable from the autumn crocus, Colchicum autumnale, it is less toxic than olchicine and is used as an antineoplastic.

Cell synchronization agent; for chromosome visualization; to induce oocyte enucleation for somatic cell cloning.

Colcemid is a colchicine (Item No. 9000760) derivative that inhibits tubulin polymerization as potently as colchicine (IC₅₀ = 2.1 and 2.4 μM, respectively) but is less toxic. At very low (nanomolar) concentrations, colcemid suppresses microtubule dynamicity and inhibits cell migration, while at micromolar levels it blocks microtubule assembly, arresting cells in metaphase. Mitotic block by colcemid is used to synchronize cells and for karyotyping in cytogenetic studies. Prolonged exposure to colcemid can activate p53, leading to apoptosis.

Often in karyotyping and cell cycle research it is desirable to increase the yield of mitotic cells in a particular phase of the cell cycle. This can be achieved in a variety of ways with the most popular being the use of a cell cycle synchronizing agent such as demecolcine. Demecolcine will arrest cells in metaphase with no remarkable effect on the biochemical events in mitotic cells or in synchronized G1 and S phase cells. White blood cells are often treated with demecolcine to arrest cells in metaphase.

Store at -20°C

Colcemide is purified by chromatography on silica and eluting with CHCl3/MeOH (9:1), and by recrystallisation from EtOAc/Et2O to form yellow prisms. UV in EtOH has max 243nm ( 30,200) and 350nm ( 16,3000). [Synthesis, IR, NMR, MS: Capraro & Brossi Helv Chim Acta 62 965 1979, Beilstein 8 IV 3319.]

[1] ANJUM MUZAFFAR. Antitubulin effects of derivatives of 3-demethylthiocolchicine, methylthio ethers of natural colchicinoids, and thioketones derived from thiocolchicine. Comparison with colchicinoids[J]. Journal of Medicinal Chemistry, 1990, 33 2: 567-571. DOI: 10.1021/jm00164a015
[2] C L RIEDER  R E P. Colcemid and the mitotic cycle.[J]. Journal of cell science, 1992, 102 ( Pt 3): 387-392. DOI: 10.1242/jcs.102.3.387
[3] MARY ANN JORDAN  Leslie W. Microtubules as a target for anticancer drugs[J]. Nature Reviews Cancer, 2004, 4 4: 253-265. DOI: 10.1038/nrc1317
[4] JOZEF CURLEJ  Peter C  Jozef Bulla. Occurrence of chromosomal aneuploidy in rabbit oocytes and embryos at different developmental stages.[J]. Zygote, 2010, 18 3: 203-207. DOI: 10.1017/s0967199409990207
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[7] ANNA A SABLINA. p53 activation in response to microtubule disruption is mediated by integrin-Erk signaling[J]. Oncogene, 2001, 20 8: 899-909. DOI: 10.1038/sj.onc.1204156